Toll-like receptor 3 mediates West Nile virus entry into the brain causing lethal encephalitis

By Tian Wang, T. Town, L. Alexopoulou, John F Anderson, E. Fikrig, R. Flavell. Nature Medicine, 2004

1,190 citations recorded by the source corpus.

Subfields: Infectious Diseases, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/79bd488af2cfa7dc9cf91c4a468134b0c7006ef6

How researchers see this paper

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In Infectious Diseases

1. G. Trinchieri
2. B. B. Finlay
3. G. McFadden
4. Taro Kawai
5. Shizuo Akira

In Public Health, Environmental and Occupational Health

1. Shizuo Akira
2. Taro Kawai

Citations in the corpus

• Innate immunity and neuroinflammation in the CNS: The role of microglia in Toll‐like receptor‐mediated neuronal injury (2009, background): “In agreement with this hypothesis, intracerebral infection with WNV leads to identical outcomes in wild-type and TLR3KO mice (Wang et al., 2004).”
• Therapeutic targeting of innate immunity with Toll-like receptor agonists and antagonists (2007, background): “For example, recognition of viral RNA by TLR3 drives CNS inflammation in mice infected with the West Nile viru”
• Pattern Recognition Receptors and the Innate Immune Response to Viral Infection (2011, methodology): “For instance, TLR3 deficient mice were protected compared to their wild type counterparts when challenged with a lethal dose of West Nile Virus (WNV) [34].”
• The RNA Helicase Lgp2 Inhibits TLR-Independent Sensing of Viral Replication by Retinoic Acid-Inducible Gene-I1 (2005, background): “As a control for these measurements, we monitored the production of RANTES, another IRF-3-regulated gene, after SV infection, or stimulation by ligands for the following TLRs: poly(I-C) (TLR3), LPS (TLR4), R-848 (TLR7), and two other viruses, HSV-1 (TLR9) and influenza (TLR7).”
• From blood–brain barrier to blood–brain interface: new opportunities for CNS drug delivery (2016, background): “1α,25-dihydroxyvitam D3 enhances cerebral clearance of human amyloid-β peptide(1-40) from mouse brain across the blood–brain barrier.”
• Anti-immunology: evasion of the host immune system by bacterial and viral pathogens. (2006, background): “In some cases, TLR3 can actually exacerbate viral pathogenesis (Wang et al., 2004).”
• Toll-like receptors and their crosstalk with other innate receptors in infection and immunity. (2011, background): “TLR4-deficient mice challenged with S. typhimurium are more susceptible to infection than control mice and show increased bacterial accumulation within the mesenteric lymph nodes (Weiss et al., 2004).”
• Regulation of innate immune responses in the brain (2009, background): “By contrast, the activation of TLR3 expressed by systemic myeloid cells results in TNF-mediated breakdown of the BBB and therefore is detrimental to defence against West Nile virus (WNV) encephalitis in mic”
• Viral evasion and subversion of pattern-recognition receptor signalling (2008, background): “by contrast, infection in the absence of TLR3 led to a reduced viral load and dampened inflammatory responses in the brain 99 .”
• Toll-like receptors in antiviral innate immunity (2013, background): “Furthermore, TLR3mediated inflammatory responses facilitated West Nile virus (WNV) entry into CNS via destruction of the blood brain barrier resulting in lethal encephalitis [94].”
• The blood–brain barrier in systemic infection and inflammation (2021, background): “For example, an increase in solute permeability is commonly observed in studies during which systemic inflammation is modeled by noninfective inflammatory challenges, such as administration of the bacterial cell wall component LPS [104], the double-stranded RNA molecule poly (I:C) (to simulate virus”